Elevated dopa decarboxylase activity in living brain of patients with psychosis.

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Elevated dopa decarboxylase activity in living brain of patients with psychosis. / Reith, J; Benkelfat, C; Sherwin, A; Yasuhara, Y; Kuwabara, H; Andermann, F; Bachneff, S; Cumming, P; Diksic, M; Dyve, S E; Etienne, P; Evans, A C; Lal, S; Shevell, M; Savard, G; Wong, D F; Chouinard, G; Gjedde, A.

In: Proceedings of the National Academy of Science of the United States of America, Vol. 91, No. 24, 1994, p. 11651-4.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Reith, J, Benkelfat, C, Sherwin, A, Yasuhara, Y, Kuwabara, H, Andermann, F, Bachneff, S, Cumming, P, Diksic, M, Dyve, SE, Etienne, P, Evans, AC, Lal, S, Shevell, M, Savard, G, Wong, DF, Chouinard, G & Gjedde, A 1994, 'Elevated dopa decarboxylase activity in living brain of patients with psychosis.', Proceedings of the National Academy of Science of the United States of America, vol. 91, no. 24, pp. 11651-4.

APA

Reith, J., Benkelfat, C., Sherwin, A., Yasuhara, Y., Kuwabara, H., Andermann, F., Bachneff, S., Cumming, P., Diksic, M., Dyve, S. E., Etienne, P., Evans, A. C., Lal, S., Shevell, M., Savard, G., Wong, D. F., Chouinard, G., & Gjedde, A. (1994). Elevated dopa decarboxylase activity in living brain of patients with psychosis. Proceedings of the National Academy of Science of the United States of America, 91(24), 11651-4.

Vancouver

Reith J, Benkelfat C, Sherwin A, Yasuhara Y, Kuwabara H, Andermann F et al. Elevated dopa decarboxylase activity in living brain of patients with psychosis. Proceedings of the National Academy of Science of the United States of America. 1994;91(24):11651-4.

Author

Reith, J ; Benkelfat, C ; Sherwin, A ; Yasuhara, Y ; Kuwabara, H ; Andermann, F ; Bachneff, S ; Cumming, P ; Diksic, M ; Dyve, S E ; Etienne, P ; Evans, A C ; Lal, S ; Shevell, M ; Savard, G ; Wong, D F ; Chouinard, G ; Gjedde, A. / Elevated dopa decarboxylase activity in living brain of patients with psychosis. In: Proceedings of the National Academy of Science of the United States of America. 1994 ; Vol. 91, No. 24. pp. 11651-4.

Bibtex

@article{eeaf3070b31411debc73000ea68e967b,
title = "Elevated dopa decarboxylase activity in living brain of patients with psychosis.",
abstract = "The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.",
author = "J Reith and C Benkelfat and A Sherwin and Y Yasuhara and H Kuwabara and F Andermann and S Bachneff and P Cumming and M Diksic and Dyve, {S E} and P Etienne and Evans, {A C} and S Lal and M Shevell and G Savard and Wong, {D F} and G Chouinard and A Gjedde",
year = "1994",
language = "English",
volume = "91",
pages = "11651--4",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "The National Academy of Sciences of the United States of America",
number = "24",

}

RIS

TY - JOUR

T1 - Elevated dopa decarboxylase activity in living brain of patients with psychosis.

AU - Reith, J

AU - Benkelfat, C

AU - Sherwin, A

AU - Yasuhara, Y

AU - Kuwabara, H

AU - Andermann, F

AU - Bachneff, S

AU - Cumming, P

AU - Diksic, M

AU - Dyve, S E

AU - Etienne, P

AU - Evans, A C

AU - Lal, S

AU - Shevell, M

AU - Savard, G

AU - Wong, D F

AU - Chouinard, G

AU - Gjedde, A

PY - 1994

Y1 - 1994

N2 - The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.

AB - The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.

M3 - Journal article

C2 - 7972118

VL - 91

SP - 11651

EP - 11654

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 24

ER -

ID: 14942549